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PubMed1991

Cardiovascular responses to nifedipine in anaesthetized rats with abnormal blood gas/pH levels.

1. Blood pressure and pulse rate responses to intravenously (i.v.) administered nifedipine were studied in chloralose-anaesthetized rats subjected to hypoxaemia, hyperoxaemia, alkalosis, acidosis, hypocarbia with alkalosis, or hypercarbia with acidosis. 2. Ventilation with a gas mixture of 17% O2, 28% O2, or 23% O2 with 5% CO2 at a fixed stroke volume (10 mL/kg) and rate (80 strokes/min) induced hypoxaemia, hyperoxaemia or hypercarbia, respectively. Hypocarbia was induced by ventilation with 17% O2 at 160 strokes/min. Acidosis or alkalosis was produced by intravenous infusion of 1 mol/L HCl or 1 mol/L NaHCO3, respectively, in animals ventilated with room air. 3. There were significant decreases in blood pressure and pulse rate during acidosis, and increases in pulse rate during alkalosis and hypercarbia. No marked changes in these parameters were observed under the other experimental conditions. 4. The control animals showed a dose-dependent decrease in blood pressure without marked changes in pulse rate in response to nifedipine injection. 5. Significant reductions in the hypotensive effect of nifedipine were observed in rats subjected to alkalosis, acidosis, or hypercarbia. A similar tendency was also found during hypocarbia while the responses to nifedipine during hypoxaemia and hyperoxaemia were statistically the same as those in the controls. 6. It is concluded that alterations of blood pH reduce the hypotensive effect of nifedipine, and we suggest that blood pH changes probably play a more important role than PO2 or PCO2 abnormalities in altering the cardiovascular responses to nifedipine in hypoventilated or hyperventilated rats.

Acidosis↗
PubMed1986

Influence of heat exposure on acid/base and fluid balance in hyperhydrated goats.

Hyperhydrated goats were exposed to an environmental temperature of 45 degrees C (relative humidity 70%) for 120 min. After 90 min, rectal temperature and respiratory frequency reached plateau levels of 40.5 degrees C and 280 respirations min-1, respectively. Measurements of arterial and venous blood acid-base parameters revealed that respiratory alkalosis had started to develop after 60 min, and had become obvious at the end of the heat exposure period. Renal compensation (evidenced by gradual increases in urinary pH and renal Na excretion) developed in parallel with the respiratory alkalosis. The heat exposure elicited a moderate, temporary inhibition of the water diuresis, but no obvious increase in the renal excretion of arginine vasopressin (antidiuretic hormone, ADH). Preliminary determinations of plasma aldosterone did not show any change during the actual heat exposure period, but a 50% temporary decrease in plasma aldosterone 30 min thereafter. The study confirms the susceptibility of goats to develop respiratory alkalosis during thermoregulatory panting, and shows that this is not to any appreciable extent diminished during hyperhydration. It can further be concluded that a heat-induced rise in body temperature to 40.5 degrees C is no powerful stimulus for vasopressin release in the hyperhydrated goat. The determinations of plasma aldosterone suggest that reduced liberation of the hormone does not contribute to the immediate renal compensation of respiratory alkalosis, but that respiratory alkalosis reaching a certain intensity inhibits aldosterone secretion.

Acid-Base Equilibrium↗
PubMed1975

Hydrocortisone restoration of the pH-dependent metabolic responses to catecholamines.

Feeding NH4CL to fasted rats caused changes of blood levels of lactate, glycerol, and insulin, hepatic levels of glycogen and phosphorylase, and muscle levels of glycogen and glucose 6-P in the direction opposite to the changes induced by respiratory alkalosis. The effects of epinephrine and isoproterenol in vivo on these metabolic indices, which are classified as their function mediated via the adrenegic beta receptor, were potentiated by NH4CL feeding in contrast to their attenuation in alkalosis. The prior treatment of the rat with hydrocortisone was very effective in overcoming the alkalosis-induced inhibition of the beta-receptor-mediated metabolic actions of epinephrine and isoproterenol, such as the activation of liver phosphorylase, accumulation of muscle hexose phosphates, and stimulation of pancreatic secretion of insulin. Epinephrine sensitivity of the liver and muscle levels of cyclic AMP was not altered by the hydrocortisone therapy or inductions of alkalosis and acidosis. The mechanism for the hydrocortisone restoration of the adrenergic beta functions in alkalosis is discussed as related to its permissive effect.

Acidosis↗
PubMed1989

Surface EMG power spectrum and intramuscular pH in human vastus lateralis muscle during dynamic exercise.

The relationship between intramuscular pH and the frequency components of the surface electromyographic (EMG) power spectrum from the vastus lateralis muscle was studied in eight healthy male subjects during brief dynamic exercise. The studies were carried out in placebo control and metabolic alkalosis induced by oral administration of NaHCO3. At the onset of exercise, blood pH was 0.08 units higher in alkalosis compared with placebo. Muscle lactate accumulation during exercise was higher in alkalosis (32 +/- 5 mmol/kg wet wt) than in placebo (17 +/- 4 mmol/kg wet wt), but no difference in intramuscular pH was found between the two conditions. The EMG power spectrum was shifted toward lower frequencies during fatigue in the control condition (10.1 +/- 0.9%), and these spectral shifts, evaluated from changes in the mean power frequency (MPF) of the EMG power spectrum, were further accentuated in alkalosis (19 +/- 2%). Although the changes in frequency components of EMG correlated with muscle lactate accumulation (r = 0.68, P less than 0.01), no direct relationship with muscle pH was observed. We conclude that alkalosis results in a greater reduction in MPF associated with a higher muscle lactate accumulation. However, the good correlation observed between the two variables is not likely causative, and a dissociation between intramuscular pH and the increase in the low-frequency content of EMG power spectrum appears during muscle fatigue.

Adult↗
PubMed2004

The meaning of acid-base abnormalities in the intensive care unit: part III -- effects of fluid administration.

Stewart's quantitative physical chemical approach enables us to understand the acid-base properties of intravenous fluids. In Stewart's analysis, the three independent acid-base variables are partial CO2 tension, the total concentration of nonvolatile weak acid (ATOT), and the strong ion difference (SID). Raising and lowering ATOT while holding SID constant cause metabolic acidosis and alkalosis, respectively. Lowering and raising plasma SID while clamping ATOT cause metabolic acidosis and alkalosis, respectively. Fluid infusion causes acid-base effects by forcing extracellular SID and ATOT toward the SID and ATOT of the administered fluid. Thus, fluids with vastly differing pH can have the same acid-base effects. The stimulus is strongest when large volumes are administered, as in correction of hypovolaemia, acute normovolaemic haemodilution, and cardiopulmonary bypass. Zero SID crystalloids such as saline cause a 'dilutional' acidosis by lowering extracellular SID enough to overwhelm the metabolic alkalosis of ATOT dilution. A balanced crystalloid must reduce extracellular SID at a rate that precisely counteracts the ATOT dilutional alkalosis. Experimentally, the crystalloid SID required is 24 mEq/l. When organic anions such as L-lactate are added to fluids they can be regarded as weak ions that do not contribute to fluid SID, provided they are metabolized on infusion. With colloids the presence of ATOT is an additional consideration. Albumin and gelatin preparations contain ATOT, whereas starch preparations do not. Hextend is a hetastarch preparation balanced with L-lactate. It reduces or eliminates infusion related metabolic acidosis, may improve gastric mucosal blood flow, and increases survival in experimental endotoxaemia. Stored whole blood has a very high effective SID because of the added preservative. Large volume transfusion thus causes metabolic alkalosis after metabolism of contained citrate, a tendency that is reduced but not eliminated with packed red cells. Thus, Stewart's approach not only explains fluid induced acid-base phenomena but also provides a framework for the design of fluids for specific acid-base effects.

Acid-Base Equilibrium↗
PubMed1995

Influence of changed blood pH on anionic sites in the labyrinth.

Using polyethyleneimine as a cationic probe, changes in the anionic sites of the labyrinthine basal laminae occurred during acidosis and alkalosis. Hartley-strain guinea pigs (200-300 g) with normal Preyer's reflex were injected i.v. with 0.5% polyethyleneimine (PEI, mol. wt 1800) solution adjusted to pH 7.3 with HCI via an axillary vein. The animals were divided into three groups: control, acidosis, and alkalosis. Acidosis was produced by inducing hypoxia, and alkalosis by injecting 7% NaHCO3. In controls, anionic sites were demonstrated on the basal laminae in the labyrinth. During both acidosis and alkalosis, a decreased number of anionic sites were observed on the basal laminae of the capillary walls in both stria vascularis and subepithelial layer of the vestibular sensory epithelium. However, an increase in anionic sites was observed on the basal lamina in Reissner's membrane during both acidosis and alkalosis.

Acidosis↗
PubMed1998

pHo, pHi, and PCO2 in stimulation of IP3 and [Ca2+]c in piglet cerebrovascular smooth muscle.

Hypocapnia produces cerebral vasoconstriction. The mechanisms involved in hypocapnia-induced elevation of vascular smooth muscle tone remain unclear. We addressed the hypothesis that, in cerebrovascular smooth muscle, increases in extracellular pH (pHo) cause increases in Ins(1,4,5)P3 and cytosolic calcium ([Ca2+]c). Superfused primary cultures of piglet cerebral microvascular smooth muscle cells were exposed to artificial CSF (aCSF) of control (pHo 7. 4, PCO2 36 mm Hg), metabolic alkalosis (pHo 7.7, PCO2 36 mm Hg), or respiratory alkalosis (pHo 7.7, PCO2 19 mm Hg). Intracellular pH (pHi) and [Ca2+]c were measured, using BCECF and fura-2, respectively, with dual wavelength spectroscopy. Ins(1,4,5)P3 was determined by a protein binding assay. Both metabolic and respiratory acidosis treatments increased pHi from the control value of about 7.2 to 7.35. Metabolic and respiratory alkalosis increased Ins(1,4,5)P3, as we showed previously. Metabolic and respiratory alkalosis increased [Ca2+]c about 80% and 110%, respectively. Neither Ins(1,4,5)P3 nor [Ca2+]c increased in cells treated with aCSF that produced control pHo with increased pHi (7.3). In contrast, when pHo increased (7.7), but pHi was maintained at control (7.2), Ins(1,4,5)P3 increased from 123 pmol/well to 307 pmol/well and [Ca2+]c increased 46%. However, the increase of [Ca2+]c was less than with either respiratory or metabolic alkalosis. Thus, hypocapnia-induced cerebral vasoconstriction could involve production of Ins(1,4,5)P3 with resultant elevation in [Ca2+]c. While the Ins(1,4,5)P3 signal appears to be dependent on an increase in extracellular pH, a role for intracellular pH cannot be completely excluded.

Alkalosis, Respiratory↗
PubMedDate not supplied

[Role of the acid-base status on the changes of haemoglobin oxygen affinity in arterial hypoxemia (author's transl)].

Fifty-seven patients, all with chronic respiratory insufficiency and hypoxemia, have been classified in five groups according to their acid-base status, determined by the intra-erythrocytic pH (pHi) : A. normal acid-base balance ; B. chronic alkalosis ; C. acute alkalosis ; D. acute acidosis ; E. chronic acidosis. We have measured in the arterial blood : Po2, PCO2, plasmatic pH (pHp1), pHi, P50(7,40) and 2,3-DPG. From these values. the base-excess (B.E.) and the P50 to real pH [P50 I.V.] have been computed. There is a good correlation between 2,3-DPG and P50 (r = 0.707), none between P50 and Pao2. For a normal acid-base balance, P50 and 2.3-DPG also are normal. Increased in chronic alkalosis, the amount of DPG is decreased in chronic acidosis. The DPG-pHi correlation is very good (r = 0.691 ; pless 0.001) and the changes of the acid-base balance seem to be the main factors for controlling the DPG synthesis : it increases it in chronic alkalosis and reduces it in chronic acidosis. Thus the P50(I.V.) returns to the normal range on account of the Bohr effect adjustement. On the contrary, in acute acidosis and alkalosis, the amount of DPG is normal and the P50(I.V.) is increased or reduced. Therefore the duration of the acid-base lack of balance also interfers.

Acid-Base Equilibrium↗
PubMedDate not supplied

Acid-base and electrolyte abnormalities in febrile patients with bacteraemia.

OBJECTIVES: Very commonly febrile patients with bacteraemia develop a variety of acid-base and electrolyte disturbances which play a significant role in the morbidity and mortality of these patients. This study was undertaken to describe the pathogenetic mechanisms of these abnormalities in febrile patients with bacteraemia. METHODS: Fifteen febrile patients with bacteraemia, aged 24-62 years, were studied. In all patients blood cultures revealed Gram-negative rods. None of them had septic shock, diabetes mellitus, renal or liver failure and none was receiving drugs influencing acid-base balance and electrolyte levels or was a heavy alcohol consumer. RESULTS: Nine patients had respiratory alkalosis, which was possibly due to bacterial toxins, while the remaining 6 had a wide-gap metabolic (lactic) acidosis coexisting with respiratory alkalosis. Hypokalaemia was found in four patients and was mainly due to respiratory alkalosis. However, kaliuria due to hypomagnesaemia contributed to hypokalaemia in 2 patients. Hypomagnesaemia was detected in 3 patients and was attributed to respiratory alkalosis as well as to magnesiuria induced by metabolic acidosis or phosphate depletion. Hypophosphataemia was found in 5 patients who also had respiratory alkalosis and/or phosphaturia due to metabolic acidosis or hypomagnesaemia. Finally, one patient had multifactorial origin hypocalcaemia. CONCLUSION: Febrile patients with bacteraemia develop a number of acid-base and electrolyte disturbances attributed to various pathogenetic mechanisms.

Acid-Base Imbalance↗
PubMed1981

Interregional differences in brain intracellular pH and water compartmentation during acute normoxic and hypoxic hypocapnia in the anesthetized dog.

Interregional differences in intracellular pH (pHi) in brain tissue, and its regulation following 1 and 5 h of respiratory alkalosis (with and without hypoxemia) were determined in N2O anesthetized dogs. Two techniques for pHi estimation were used (TCO2 and 14C-DMO) and included corrections for measured extracellular fluid (35SO4(2-)) space (ECS). Cortical pHi by the two techniques agreed closely in control and in 3 of the 4 experimental conditions, suggesting: (a) our estimation of extracellular fluid (ECF) [HCO3-] from measured CSF [HCO3-] was a valid assumption; and (b) our method had sufficient resolution to determine the magnitude of brain pHi regulation during respiratory acid-base disturbances. When moderate normoxic respiratory alkalosis (PaCO2 approximately 25 mm Hg) was imposed for 5 h, pHi (in most brain regions) was well regulated and always exceeded the incomplete regulation noted in bulk CSF. When moderate hypoxemia (PaO2 approximately 45 mm Hg) accompanied hypocapnia, pHi was more closely regulated during the early phase (1 h) of respiratory alkalosis. Increased levels of metabolic acids (especially lactic acid) were critical to brain pHi regulation during the initial hour of respiratory alkalosis and accounted for much of the independent effect of hypoxemia on pHi regulation. However, these metabolic acids remained unchanged as pHi was more completely regulated between 1 and 5 h of continued hypocapnia or hypoxic hypocapnia. This time-dependent regulation of pHi may involve some regulatory role for changed transmembrane fluxes of H+ and/or HCO3-. Significant interregional differences were observed in both pHi and in ECS; with tendencies toward more alkaline pHi and lower ECS in brain stem and white matter. With respiratory alkalosis ECS fell and intracellular fluid increased in both cortex and caudate nucleus, possibly reflecting an osmotic effect of increased metabolic acid levels or reduction in cell membrane ion pumping.

Acid-Base Equilibrium↗
PubMedDate not supplied

Acid-base disorders in hyperglycemia of insulin-dependent diabetic patients on chronic dialysis.

The authors studied hyperglycemia occurring in insulin-dependent diabetic patients on chronic dialysis to determine the types of associated acid-base disorders, their treatment, and any differences from hyperglycemia in diabetic patients with intact renal function. Eighty-eight episodes of serum glucose greater than 25 mmol/L were observed, 23 in hemodialysis patients and 65 in patients on continuous peritoneal dialysis. Treatment consisted of low-dose insulin in 77 episodes and low-dose insulin plus saline in 11; no base was administered. Seventeen episodes (19%) presented with ketoacidosis. Arterial blood gas determinations were carried out at presentation in 37 of the episodes without ketoacidosis. Of these, 12 had respiratory alkalosis, six had respiratory acidosis and severe pulmonary edema, 14 had other single or mixed acid-base disorders, and only five had normal acid-base status. Insulin corrected the ketoacidosis in all instances and both pulmonary edema and respiratory acidosis in five of six instances. In eight cases metabolic alkalosis developed during treatment, without external acid loss. At the completion of treatment respiratory alkalosis was present in half the cases. No difference was noted between patients treated with hemodialysis or peritoneal dialysis. Insulin alone is sufficient for the management of hyperglycemia in dialysis patients. Certain acid-base disorders persist, but do not need further treatment. Hyperglycemia in patients on dialysis is characterized by infrequent development of metabolic acidosis and frequent presentation with respiratory alkalosis, by respiratory acidosis that is corrected by insulin, and by metabolic alkalosis developing during treatment without external cause.

Acid-Base Imbalance↗
PubMed1976

Acid-base equilibrium in Menière's disease.

57 patients suffering from Meiere's disease have been examined: metabolic alkalosis has been found in 39 and metabolic acidosis in 4. Electrolytes (Na, K and Cl) were normal. Among the 31 subjects in the control series a slight metabolic alkalosis qas detected only twice. Follow-up of several patients, from one to three years, resulted in a realization of a parallel between metabolic disturbance and Meniere symptoms. A provocation test, by sodium bicarbonate oral administration, has beem attempted twice: in both instances alkalosis did increase strongly but, only once, vertigo was elicited. Meniere patients found in alkalosis were given acidifying drugs to normalize their acid-base equilibrium. Such treatment proved effective in preventing acute cochleo-vestibular crises and in improving tinnitus and deafness (in the fluctuating stage). On the interruption of treatment symptoms reappeared. The physiological-pathological significance of metabolic alkalosis in Meniere's disease still remains unclear and, consequently, this can be considered merely a predisposing factor in endolymphatic hydrops.

Acid-Base Equilibrium↗
PubMed2000

Clinical assessment of acid-base status: comparison of the Henderson-Hasselbalch and strong ion approaches.

The traditional approach for clinically assessing acid-base status uses the Henderson-Hasselbalch equation to categorize 4 primary acid-base disturbances: respiratory acidosis (increased PCO2), respiratory alkalosis (decreased PCO2), metabolic acidosis (decreased extracellular base excess or actual HCO3- concentration), and metabolic alkalosis (increased extracellular base excess or actual HCO3- concentration). The anion gap is calculated to detect unidentified anions in plasma. This approach works well clinically and is recommended for use whenever serum total protein, albumin, and phosphate concentrations are approximately normal. However, because the Henderson-Hasselbalch approach is more descriptive than mechanistic, when these concentrations are markedly abnormal the Henderson-Hasselbalch equation frequently provides erroneous information as to the cause of an acid-base disturbance. The new quantitive physicochemical approach to evaluating acid-base balance uses the simplified strong ion model to categorize 6 primary acid-base disturbances: respiratory acidosis (increased PCO2), respiratory alkalosis (decreased PCO2), strong ion acidosis (decreased strong ion difference), strong ion alkalosis (increased strong ion difference), nonvolatile buffer ion acidosis (increased plasma concentrations of albumin, globulins, or phosphate), and nonvolatile buffer ion alkalosis (decreased plasma concentrations of albumin, globulins, or phosphate). The strong ion gap is calculated to detect unidentified anions in plasma. The simplified strong ion approach works well clinically and is recommended for use whenever serum total protein, albumin, or phosphate concentrations are markedly abnormal. The simplified strong ion approach is mechanistic and is therefore well suited for describing the cause of any acid-base disturbance.

Journal Article↗
PubMed1999

Effect of liver disease and transplantation on urea synthesis in humans: relationship to acid-base status.

It has been suggested that hepatic urea synthesis, which consumes HCO-3, plays an important role in acid-base homeostasis. This study measured urea synthesis rate (Ra urea) directly to assess its role in determining the acid-base status in patients with end-stage cirrhosis and after orthotopic liver transplantation (OLT). Cirrhotic patients were studied before surgery (n = 7) and on the second postoperative day (n = 11), using a 5-h primed-constant infusion of [15N2]urea. Six healthy volunteers served as controls. Ra urea was 5.05 +/- 0.40 (SE) and 3.11 +/- 0.51 micromol. kg-1. min-1, respectively, in controls and patients with cirrhosis (P < 0. 05). Arterial base excess was 0.6 +/- 0.3 meq/l in controls and -1.1 +/- 1.3 meq/l in cirrhotic patients (not different). After OLT, Ra urea was 15.05 +/- 1.73 micromol. kg-1. min-1, which accompanied an arterial base excess of 7.0 +/- 0.3 meq/l (P < 0.001). We conclude that impaired Ra urea in cirrhotic patients does not produce metabolic alkalosis. Concurrent postoperative metabolic alkalosis and increased Ra urea indicate that the alkalosis is not caused by impaired Ra urea. It is consistent with, but does not prove, the concept that the graft liver responds to metabolic alkalosis by augmenting Ra urea, thus increasing HCO-3 consumption and moderating the severity of metabolic alkalosis produced elsewhere.

Acid-Base Equilibrium↗
PubMed1992

Citrate anticoagulation and dialysate with reduced buffer content in chronic hemodialysis.

Anticoagulation with trisodium citrate (510 mmol/l) at a rate of 126 ml/h in combination with a calcium-free, 35 mmol/l acetate dialysate and i. v. supplementation of calcium chloride (350 mmol/l) at a rate of 22.5 ml/h has been performed in renal failure patients at risk of bleeding or actively bleeding. Short-term use-i. e. on the average four dialyses in 15 patients-showed no adverse effects or clotting phenomena. However, long-term use-i. e. at least four weeks and on average sixteen dialyses in six chronic hemodialysis patients-caused paresthesias and muscular cramps possibly due to the combination of insufficient calcium supplementation and metabolic alkalosis. To prevent metabolic alkalosis, the acetate content of the dialysate and the infusion rate of citrate were reduced to 29.5 mmol/l and 100 ml/h, respectively. To prevent clotting at this infusion rate, a calcium and magnesium-free dialysate was used and i. v. supplementation of calcium chloride (350 mmol/l) and magnesium chloride (250 mmol/l) was performed at rates of 30 ml/h and 15 ml/h, respectively. Six chronic renal failure patients were dialyzed with this regimen for an average of four months. There were no side effects or metabolic alkalosis noted. When an equimolar amount of bicarbonate replaced the acetate in the calcium and magnesium-free dialysate, side effects and metabolic alkalosis were seen within three dialyses. When the bicarbonate concentration in the dialysate was reduced to 25 mmol/l neither side effects nor metabolic alkalosis was observed. Thus citrate anticoagulation in patients on chronic hemodialysis can only be performed when the buffer content of the dialysate is reduced.

Acetates↗
PubMed1992

[Optimal pH and PaCO2 during moderate hypothermia].

Effects of pH and PaCO2 on cerebral as well as systemic hemodynamics and oxygen consumption were investigated during moderate hypothermia under 0.5% halothane anesthesia. Twenty-seven adult mongrel dogs were cooled to 28 degrees C (brain temperature) with a surface cooling method. They were divided into 3 groups, pH-stat (pH 7.35 n = 9), alpha-stat (pH 7.48 n = 9), and alkalosis (pH 7.70 n = 9). During hypothermia cardiac index fell to 74%, 56%, and 45%, and cerebral blood flow to 54%, 42%, and 36% in pH-stat, alpha-stat and alkalosis groups, respectively. Cerebral and systemic oxygen consumptions decreased to approximately 54% and 47%, respectively in all groups. Cerebrospinal fluid pH rose from 7.36 precooling to 7.49 (pH-stat), 7.53 (alpha-stat), and 7.72 (alkalosis). We concluded from these results that pH-stat and alpha-stat management have no significant effect on either hemodynamics or metabolism during moderate hypothermia but alkalosis management has deleterious effects because of the alkalinity itself and of the hyperventilation by which the alkalosis is induced.

Animals↗
PubMed1975

The effect of acid-base balance on neostigmine antagonism of d-tubocurarine-induced neuromuscular blockade.

d-Tubocurarine (dTc) was infused intravenously into 35 cats anesthetized with chloralose and urethane at a constant continuous rate to produce and maintain 90 per cent depression of twitch height of the anterior tibial muscle following supramaximal stimulation of the peroneal nerve. The mean infusion rates that produced 90 per cent depression were not significantly altered by respiratory acid-base changes. Metabolic alkalosis decreased (32.5 per cent) and metabolic acidosis increased (27.7 per cent) the required infusion rate of dTc. When pH and Paco2 were maintained at 7.37 and 38 torr, respectively, the addition of a bolus of neostigmine, 10.5 mug/kg, intravenously, to the continuing infusion of dTc produced 50 per cent antagonism of the dTc-depressed twitch. Respiratory alkalosis and metabolic acidosis did not alter the dose of neostigmine needed to produce 50 per cent antagonism. However, during respiratory acidosis (pH 7.13, Paco2 66 torr) and metabolic alkalosis (pH 7.59, Paco2 36 torr) 20.0 and 18.0 mug/kg neostigmine, respectively, were needed to produce 50 per cent antagonism. Still larger doses of neostigmine (75 mug/kg) could not completely antagonize the block unless pH and Paco2 were returned to 7.30-7.50 and 35-45 torr, respectively. It is concluded that respiratory acidosis and metabolic alkalosis limit and oppose antagonism of dTc by neostigmine.

Acid-Base Equilibrium↗
PubMed1978

Determinants of oxygen uptake during sodium bicarbonate infusion.

Steady-state passive hyperventilation alkalosis produces a predictable increase in oxygen uptake (VO2) proportional to the change in arterial pH (pHa) while variable changes in VO2 have been reported during alkali infusion. To compare metabolic with respiratory alkalosis 17 dogs were anesthetized with halothane and their VO2 response to respiratory alkalosis evaluated by hyperventilation. The pHa measured during this phase was duplicated during the later continuous infusion of NaHCO3 at which time either 1) ventilation was held constant at the control level, allowing arterial carbon dioxide tension (PaCO2) to rise as a consequence of the bicarbonate dissociation, or 2) PaCO2 was held constant by servo control of ventilation. Hyperventilation (pHa 7.6, PaCO2 13 Torr) produced an average increase in VO2 of 24%. During the bicarbonate infusion at constant ventilation (pHa 7.6, PaCO2 45 Torr) VO2 increased only 7%; however, when PACO2 was held constant by servo ventilation VO2 increased 21% above control. We conclude that respiratory and metabolic alkalosis produce similar increases in VO2 when steady-state acid-base conditions are achieved.

Alkalosis↗